Why the study?
This review describes the impact of endurance and strength physical training on the cardiovascular system, examining molecular signaling pathways, muscle adaptations, and metabolic, cardiac remodeling, and hemodynamic changes.
This review highlights the distinct molecular signaling pathways and cardiac adaptations, such as eccentric versus concentric hypertrophy, induced by endurance and strength training.
The purpose of this review is to describe the impact of endurance and strength physical training on the cardiovascular system by reviewing the molecular signaling pathways, which plays a key role in different muscle adaptations, and the cardiac changes in terms of metabolic and cardiac remodeling, and hemodynamics. In response to endurance-exercise, multiple signaling pathways, including Ca²⁺-dependent pathways, reactive oxygen species (ROS), AMP-dependent protein kinase (AMPK), and mitogen activated protein kinases (p38 MAPK), are involved in the regulation of peroxisome-proliferator-activated receptor-γ coactivator-1α (PGC-1α), which controls the mitochondrial biogenesis. Strength training increases the insulin-like growth factor (IGF-1) which initiates the phosphatidylinositol 3-kinase (PI3-k)-(AKT)-(mTOR) signaling cascade, resulting in the synthesis of proteins and the muscle hypertrophy. In addition to the well-documented changes in skeletal muscle, a critical component of the response to exercise training is the dynamic cardiac remodeling, which is classified as either pathological or physiological depending on triggers.
No takes yet. Share an insight, caveat, or question.
Toktarbay et al. (2023) conducted a review in Cardiovascular adaptations to exercise. Exercise (endurance and strength training) was evaluated.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: